Glutamate modulation of physiological and behavioral responses to restraint stress: Participation of supraoptic nucleus of the hypothalamus

Abstract

AIMS: Acute restraint stress (RS) has been reported to activate the supraoptic nucleus of the hypothalamus (SON). The aim of the present study was to evaluate the role of glutamatergic neurotransmission in the SON on autonomic [mean arterial pressure (MAP), heart rate (HR), and tail cutaneous temperature], neuroendocrine (plasma levels of corticosterone, oxytocin, and vasopressin), and behavioral responses to RS. METHODS: Male Wistar rats with bilateral SON cannulas received microinjections of NMDA or non-NMDA receptor antagonists or vehicle before restraint stress, and the effects on cardiovascular, tail temperature, hormonal, and behavioral responses were evaluated RESULTS: Microinjection of DL-AP7 or NBQX into the SON reduced MAP increases and tail temperature decreases induced by RS. Also, NBQX enhanced RS-evoked tachycardia. SON treatment with DL-AP7 or NBQX reduced RS-induced increases in oxytocin, without affecting vasopressin plasma levels. Morever, NBQX enhanced RS-induced increases in plasma corticosterone level. DL-AP7 inhibited the RS-caused delayed anxiogenic-like effect. CONCLUSION: NMDA and non-NMDA glutamate receptors in the SON facilitate pressor response and oxytocin release during RS. In addition, non-NMDA receptors exert an inhibitory influence RS-induced increases in heart rate and corticosterone release, whereas NMDA receptors contribute to the delayed expression of anxiety-like behaviors.